Brain Damage

Introduction

MR imaging is the most sensitive clinical tool to de- tect brain abnormalities caused by different types of damage while neuropathological evaluation remains most specific. MR imaging is not optimal to deter- mine the etiology of brain damage, but it has certain- ly broadened our perspective on many traumatic brain injuries. One single etiology often results in multiple different types of brain injury depending on the patient’s age at the time of the injury and the du- ration of the injury. Brain injury includes a broad spectrum of conditions such as hypoxic ischemic en- cephalopathy (HIE, or anoxic ischemic encephalopa- thy, AIE), accidental brain trauma, but also nonacci- dental brain trauma (child abuse). Besides direct trauma, metabolic and cerebrovascular alterations can also cause brain damage.

Newer neuroimaging modalities such as diffusion, perfusion and spectroscopy are natural components of today’s neuroradiology practice. This has necessi- tated the expansion of competence from the tradi- tional anatomical knowledge to a broad understand- ing of the underlying physiology and pathophysiolo- gy.

In the critically ill neonate, hypoxia, anoxia and is- chemia all contribute to the brain damage and the imaging findings. When the neonatal brain is ex- posed to severe hypoxia, anoxia or ischemia, the de- veloping brain undergoes a number of metabolic and structural changes, which can be monitored by MR imaging and MR spectroscopy. MR spectroscopy is capable of measuring metabolites in this damaging cascade, such as excess release of excitatory neuro- transmitters (glutamine and glutamate) at synaptic junctions leading to neurotoxicity. Excess lactate can also be measured. In an older child’s brain the decline of N-acetylaspartate (NAA) has been associated with anoxia. NAA, however, is not a good marker in a very young brain since it is normally quite low in infants and young children and therefore a decline cannot be

reliably visualized. In older children a decrease in NAA provides a good landmark for brain damage.

Lactate can be significantly increased early in the anoxic event, but it is not a persistent finding even with severe brain injury.

Vascular autoregulation in the preterm child is dif- ferent from that in a term child or an older child.Also the vascular arrangement in the preterm infant (<34weeks) is different from that in the term infant.

The concept of “diving reflex” in which hypoxia or anoxia results in rearrangement of the blood from less vital body structures to the more vital structures such as the brain and specifically to the basal ganglia and brain stem. This will help to minimize damage to these structures. In preterm children the autoregula- tion reflexes are immature or absent, and any signifi- cant drop in systemic pressure will result in de- creased perfusion of the brain. This may lead to deep white matter damage. Periventricular leukomalacia (PVL) results from ischemic damage of periventricu- lar white matter and it is often seen in preterm in- fants but not in term infants. In preterm infants ger- minal matrix hemorrhages and venous infarctions leading to hemorrhage are also seen. In term infants HIE may lead to multicystic leukomalacia of various degrees of severity.

Early ischemia is difficult to detect in MR images since the normal neonatal brain demonstrates T2 hy- perintensity due to lack of myelination in this stage of development. However, diffusion imaging detects early hypoxic and ischemic events leading to cytotox- ic edema and later to volume loss. Cerebrovascular occlusion with stroke in the neonate is more preva- lent than previously recognized. In the preterm in- fant, most CNS ischemic injuries result in PVL. Brain infarctions with or without hemorrhage can occur in the term infant following HEI but also as a complica- tion of sepsis or hypercoagulable state.

Though CT remains the main modality in assess- ing the patient with acute head trauma, MR imaging adds a new dimension to the diagnosis. In the sus- pected cases of nonaccidental trauma, MR imaging is

Brain Damage

In collaboration with Lawrence Buadu

a sensitive modality not only in the evaluation of the presence of the trauma but also in the estimation of the timing of the trauma, the patient’s prognosis and the extent of the trauma. However, one should re- member that interpretation on pediatric neuroimag- ing studies always requires clinical correlation.

Nonaccidental Trauma

Scalp Injury (Subgaleal Hemorrhage) Clinical Presentation

A 3-month-old child presenting with decreased re- sponsiveness and suspected nonaccidental head in- jury.

Images (Fig. 7.1)

A. Sagittal T2-weighted image demonstrates scalp soft tissue swelling consistent with subgaleal hem- orrhage

B. In addition to the low signal scalp hematoma, bi- lateral subdural low signal collections are also demonstrated on coronal FLAIR image. These could represent chronic subdural hematomas or hygromas

Figure 7.1

Scalp injury (subgaleal hemorrhage)

A B

Skull Fracture Clinical Presentation

A 2-month-old female status after a recent fall.

Images (Fig. 7.2)

A. CT scan shows a right parietal skull fracture with overlying soft tissue swelling (arrow)

B. The fracture is seen to better advantage on the lat- eral plain skull radiograph (arrow)

A

B

Figure 7.2

Skull fracture

Subdural Hemorrhage Clinical Presentation

A 2-month-old admitted with seizures. Ophthalmo- logic examination revealed retinal hemorrhages.

Images (Fig. 7.3)

A. Coronal FLAIR image shows bilateral subdural hemorrhages in different stages of temporal evo- lution. Although not conclusive, it suggests repeti- tive trauma

B. The finding of hemorrhagic contusion in the left parieto-occipital region (arrow) on sagittal T1- weighted image further raises the suspicion for nonaccidental head injury

C. Follow-up coronal FLAIR image several months later after reportedly minor trauma shows signifi- cant brain atrophy confirming severe brain injury at initial presentation

Figure 7.3

Subdural hemorrhage

A B

C

Subarachnoid and Subdural Hemorrhage Clinical Presentation

A 9-month-old male with suspected nonaccidental head injury and retinal hemorrhages.

Images (Fig. 7.4)

A. Sagittal T1-weighted image shows a right subdur- al hematoma

B. FLAIR image shows subarachnoid hemorrhage (arrow) in the right parietal region

Figure 7.4

Subarachnoid and subdural hemorrhage

A B

Parenchymal Hemorrhage and Ischemia Clinical Presentation

A 5-month-old female presenting with altered mental status.

Images (Fig. 7.5)

A. CT scan shows focal hemorrhagic contusion in the right frontal lobe

B. Sagittal gradient-echo image confirms the pres- ence of parenchymal hemorrhage in the right frontal lobe

C. DW image shows widespread areas of ischemia in- dicating severe traumatic brain injury

Figure 7.5

Parenchymal hemorrhage and ischemia

A B

C

Diffuse Axonal Injury (DAI) Clinical Presentation

A 14-day-old female with new onset of focal seizures.

Images (Fig. 7.6)

A. CT scan shows focal hemorrhage over the left tem- poral tip (arrow)

B. DW image reveals two punctuate foci of restricted diffusion (arrows) in the left parietal region most consistent with axonal injury

Figure 7.6

Diffuse axonal injury

A B

Hypoxic Ischemic Injury Clinical Presentation

A 14-month-old female who initially presented with vomiting and possible seizure after falling down a flight of stairs.

Images (Fig. 7.7)

A. CT scan was unremarkable except for a small sub- dural hemorrhage along the interhemispheric falx (arrows)

B. T2-weighted image confirms the presence of sub- dural hemorrhages (arrows) but is otherwise un- remarkable

C. DW image demonstrates areas of restricted diffu- sion in both cerebral hemispheres indicating hy- poxic ischemic injury

D. ADC map confirms the presence of ischemic in- jury. The hyperintense areas on DW image are hy- pointense on the ADC map consistent with cyto- toxic edema

E. The acute subdural hematoma is seen as a high signal lesion in the gradient echo image. It is bet- ter seen on T2-weighted image

Figure 7.7

Hypoxic ischemic injury

A B C

D E

Infarct

Clinical Presentation

A 2-year-old female who initially presented with re- cent seizures, resolving left hemiparesis and focal EEG changes. The first MR image at that time was normal.

Images (Fig. 7.8) A. and B.

A month later the child returned to the emergency department with a history of a fall with fractures of the right tibia and fibula. Repeat MR imaging showed multiple areas of subacute infarction on DW (A) and FLAIR (B) images (arrows)

Figure 7.8 Infarct

A B

Atrophy

Clinical Presentation

A 2-month-old female presenting with seizures and apnea.

Images (Fig. 7.9)

A. Ophthalmologic examination reveals multiple retinal hemorrhages

B. Initial CT scan demonstrates extensive cortical swelling and hypodensity with relative sparing of the basal ganglia and cerebellum, the so-called “re- versal sign” or “white cerebellum sign”

C. CT scan obtained 10days later shows marked gen- eralized cerebral atrophy and linear increased density along the gyri (arrows) corresponding to sequelae of laminar necrosis

Figure 7.9 Atrophy

A

B C

Venous Sinus Thrombosis Clinical Presentation

A 5 month old male found unresponsive. Clinically child abuse is suspected.

Image (Fig. 7.10)

A. MR venogram demonstrates absence of the supe- rior sagittal sinus consistent with sinus thrombo- sis.

Thalamic Infarcts in a Shaken Infant Syndrome Clinical Presentation

A 5-month-old female found pulseless with copious bleeding from the nose and seizing. There is clinical suspicion of shaken infant syndrome.

Images (Fig. 7.11)

A. CT scan is unremarkable

B. T1-weighted image fails to demonstrate pathology C. T2-weighted image is normal

D. On GRE image there is no blood in the parenchy- ma

E. On DW image there is high signal intensity in both thalami. There are faint areas of diffusion distur- bance also involving parts of the basal ganglia as well as the hippocampi

F. On ADC map the thalami and some basal ganglia areas are hypointense

G. Exponential image shows significant hyperinten- sity of the thalami and parts of the basal ganglia.

These areas are consistent with restricted diffu- sion and cytotoxic edema as seen in HIE

Discussion

It is estimated that in excess of 2000 children in the United States die each year as a result of child abuse.

Nonaccidental head injury (NAHI) is largely restrict- ed to children under 3years of age, with the majority occurring during the first year of life. Inflicted head injury is the most common cause of traumatic death in infancy. With inflicted head injury an accurate his- tory is rarely provided at presentation. The informa- tion most commonly reported is usually of a minor nature and the history may be vague or may vary with time. Physical examination although useful may pro- vide little insight regarding underlying brain injury.

Consequently, the diagnosis and detection of NAHI usually comes to rest on radiological imaging. Al- though no single imaging finding is specific for abuse, no other medical condition fully mimics all the features of NAHI in infants and children. If radi- ographic indicators of abuse or neglect are missed, the consequences are grave for the child who will in- variably be returned to a high-risk environment.

Terminology applied to inflicted head injury in children has varied along with the evolution in the

Figure 7.10

Venous sinus thrombosis

understanding of the underlying mechanisms. Re- gardless of terminology, most inflicted head injuries in children are of the dynamic type. Dynamic injuries may occur in either (a) direct contact trauma (when a stationary head is struck by a moving object, a mov- ing head is struck by a stationary object or when both a moving head and moving object collide) or (b) in- direct injury. Contact phenomena result in localized

distortion or a fracture of the skull, focal cortical in- jury, epidural hematoma or subdural hematoma. In contrast to direct trauma, indirect injuries are inde- pendent of skull deformation and entail inertial load- ing which occurs with sudden acceleration or decel- eration of the head. Although contact may occur with this mechanism, significant life-threatening injuries may occur without an impact. Head acceleration or

Figure 7.11

Thalamic infarcts in a shaken infant syndrome

A B C

D E F

G

deceleration results in a variety of strain deforma- tions of the skull and its contents. Shear strain defor- mation which produces disruption at tissue inter- faces is the most important mechanism in the pro- duction of intracranial injury. Furthermore the pri- mary injury occurring with these biomechanical forces may result in other pathophysiological alter- ations or secondary injury (e.g. edema, swelling, hy- poxic ischemia, herniation) and produce additional imaging findings. Other etiological factors may also result in hypoxic-ischemic injury and diffuse cere- bral swelling without significant biomechanical force. These include strangulation, suffocation by hand or pillow, and prolonged squeezing of the chest.

In these types of injury, external manifestations are minor or nonexistent. Imaging is even more crucial in elucidating severity and mechanisms of injury when the clinical history is not revealing.

Although conventional MR imaging is more sensi- tive than CT scan in detection of hematomas of vari- ous ages and areas of contusions, recent research has proven MR spectroscopy and DW imaging to be in- formative in the acute phase. MR spectroscopy may distinguish those children who have suffered more significant and long-lasting brain injury by demon- strating lactate or diffusion abnormality. This may help the clinicians more accurately identify those in- fants who have suffered severe injury, and direct treatment and social services toward these infants.

Suggested Reading

Billmire ME, Myers PA (1985) Serious head injury in infants;

accident or abuse? Pediatrics 75:340–342

Buadu L, Ekholm S, Lenane A, Moritani T, Hiwatashi A, Westes- son PL (2004) Patterns of head injury in non accidental trauma. Neurographics 3(1):article 2

Caffey J (1974) The whiplash shaken infant syndrome; manual shaking by the extremities with whiplash-induced in- tracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pedi- atrics 54:396–403

Centers for Disease Control (1990) Childhood injuries in the United States. Am J Dis Child 144:627–646

Duhaime AC, Gennarelli TA, Thibault LE, Bruce DA, Margulies SS, Wiser R (1987) The shaken baby syndrome: a clinical, pathological and biomechanical study. J Neurosurg 66:409–415

Kleinman PK (1998) Diagnostic imaging of child abuse, 2nd edn. Mosby, St Louis, pp 286–287

National Clearing House on Child Abuse and Neglect Informa- tion (2000) Child fatalities fact sheet. www.calib.com/nc- canch/pubs/factsheet/fatality.html (22 Feb 2000)

Epidural and Subdural Hematoma Epidural Hematoma (EDH)

Clinical Presentation

A 10-year-old male sustained an injury to the left side of his head after a fall from bike without a helmet. He has known skull fracture on left.

Images (Fig. 7.12)

A. Noncontrast CT scan at presentation demon- strates a shallow extraaxial bleed in left temporal area (arrow). Over the right sylvian region, a small amount of subarachnoid blood is present (arrow- head)

B. CT scan 9hours later shows a biconvex EDH in the left temporal area (arrow). The central part is low density with a bright periphery. It could be due to active bleeding at the time of the hematoma with swirling blood. The right side lesion is stable C. On CT scan 24hours later a hyperdense EDH is

seen (arrow)

D. T1-weighted image after the third CT scan shows a slightly hyperintense EDH (arrow)

E. The EDH is hyperintense on proton density image (arrow)

F. T2-weighted image shows hyperintense EDH (ar- row)

G. Coronal FLAIR image shows heterogeneous but mostly hyperintense EDH (arrow)

H. GRE image shows mixed signal hematoma (ar- row); it varies from iso- to hypointense compared to gray matter

I. b

image (SE-EPI) shows also mixed signal inten- sity in EDH (arrow)

J. DW image reveals central low signal with thin pe- ripheral layer of increased signal in EDH (arrow).

The right temporal findings are stable

Figure 7.12 A–H Epidural hematoma

A B C

D E F

G H

Subdural Hematoma (SDH) Clinical Presentation

A former 25-week gestational age premature baby, now 9-month-old girl who had 2weeks extracorpore- al membrane oxygenation therapy (ECMO) for chronic lung disease.

Images (Fig. 7.13)

A. Noncontrast CT scan shows mixed density SDH in the right occipital region (arrow)

B. Sagittal T1-weighted image 10days later shows the same SDH to be hyperintense (arrow). This is con- sistent with methemoglobin formation

C. Coronal contrast-enhanced SPGR image shows small right distal ICA with less flow (arrow). This is due to the older ECMO treatment technique where right carotid artery was cannulated and sac- rificed. The cavernous sinus on right does not fill with contrast as it is thrombosed (Note: In the cur- rent technique the carotid and jugular vessels are repaired after ECMO treatment)

D. T2-weighted image shows small flow void in the right cavernous carotid artery (arrow) that repre- sents collateral flow from left since the right carotid artery has been ligated

E. T2-weighted image shows hyperintense SDH with hemosiderin stain in the medial border of the hematoma (arrow). Note good flow void in the sagittal sinus. Low volume of white matter is pres- ent as a consequence of prematurity. The corpus callosum is thin. Myelination is seen in the poste- rior limb of the internal capsule

Discussion

EDH is an uncommon complication of head trauma in children. The potential space between the inner table of the skull and the dura is the location of this hematoma. Classically, a skull fracture that crosses a branch of the middle meningeal artery results in ar- terial bleeding that dissects the dura from the inner table. However, venous bleeding is also often the rea- son for an EDH. The characteristic appearance of the hematoma is lens shaped and it respects the sutures.

EDH can also be present without a skull fracture. Ve- nous bleeding leading to an EDH is more common in children than in adults. Direct trauma to the venous sinuses or emissary veins may be the reason for the venous bleeding. Most EDHs will be examined with CT imaging and evacuated immediately. It is rare to diagnose an EDH with MR imaging in the hyperacute phase (<24hours of bleeding). In the hyperacute phase the signal changes are due to oxyhemoglobin that is iso- to slightly hypointense to the gray matter on T1-weighted images and hyperintense on T2- weighted sequences. It is more common to diagnose EDHs in the acute or early subacute phase (24–48hours after the incident). In that time the hematoma is isointense on T1-weighted image and markedly hypointense on T2-weighted image due to deoxyhemoglobin.

Signal pattern of epidural and subdural hematoma are identical, but they may be very different from those of parenchymal or intraventricular hemor- rhage of the same duration. Acute subdural hematomas (SDH) are also mostly diagnosed by CT scan.Also acute SDH may be arterial or venous in na- ture. Injury to cortical arteries can result in accumu- lation of blood in the subdural space that will cause a

Figure 7.12 I, J Epidural hematoma

I J

mass effect. The bleeding is caused by disruption of the bridging veins coursing the subdural space be- tween the cortex and the dural sinuses. Shallow SDH are sometimes difficult to detect by CT scanning;

however, the greater sensitivity of MR imaging for soft-tissue contrast, multiplanar projections and ab- sence of beam hardening bone artifacts, increase the capability of MR imaging to detect even small SDH,

especially if they are subacute. Evolution of SDH fol- lows that of EDH and is discussed above. Oxidation of deoxyhemoglobin to intracellular methemoglobin during the subacute phase causes brightening of the signal first on T1-weighted and later on T2-weighted images as red cell lysis occurs. Chronic SDHs have signal characteristics close to that of CSF, except that they are slightly higher signal due to their protein

Figure 7.13 Subdural hematoma

A B

C D E

content. On T2-weighted images the signal of SDH closely resembles that of CSF. Unlike parenchymal hemorrhages there are no hemosiderin-laden macrophages to cause the decrease in the T2 signal.

Subdural hygromas are similar in shape to SDH.

They result from a tear in the arachnoid membrane with leaking of CSF into the subdural space. These extraaxial fluid collections closely follow the CSF sig- nal in all sequences. Differentiation of chronic SDH from hygroma is not always possible on CT scan, but MRI imaging is able to make the distinction.

Suggested Reading

Blankenberg FG, Loh N-N, Bracci P, et al (2000) Sonography, CT, and MR imaging: a prospective comparison of neonates with suspected intracranial ischemia and hemor- rhage. AJNR Am J Neuroradiol 21:213–218

Bulas DI, Taylor GA, O’Donnell RM, Short BL, Fitz CR,Vezina G (1996) Intracranial abnormalities in infants treated with extracorporeal membrane oxygenation: update on sono- graphic and CT findings. AJNR Am J Neuroradiol 17:

287–294

Fobben ES, Grossman RI, Atlas SW, Hackney DB, Goldberg HI, Zimmerman RA, Bilaniuk LT. (1989) MR characteristics of subdural hematomas and hygromas at 1.5T. AJR Am J Roentgenol 3:589–595

Lin DM, Filippi CG, Steever AB, Zimmerman RD (2001) Detec- tion of intracranial hemorrhage: comparison between gra- dient-echo and b

(SE-SPI) images obtained from diffu- sion-weighted echo-planar sequences. AJNR Am J Neuro- radiol 22:1275–1281

Contusion

Clinical Presentation

An 8-year-old male was admitted following a motor vehicle accident. Several days after admission he un- derwent MR scan to fully evaluate the extent of his in- juries.

Images (Fig. 7.14)

A. T2-weighted image reveals left frontal lobe contu- sion. A shallow subdural hemorrhage is present on left (arrow). Hyperintensity is seen in the mid- brain (arrowhead). This is more likely contusion than DAI, since it involves the dorsolateral brain surface. Soft tissue swelling and contusion is seen on the left

B. Proton density image shows the same left frontal contusion and several smaller contusions in the parenchyma and basal ganglia. Blood is seen in the left lateral ventricle. A shallow subdural hema- toma is seen on the left as high signal intensity C. Proton density image above section shown in B.

Again multiple parenchymal hemorrhagic contu- sions and DAI are seen. Blood layers are seen in the dependent portions of the lateral ventricles (ar- rows)

D. T1-weighted image shows methemoglobin in the left frontal contusion. The extraaxial hematoma is best seen in this sequence. Multiple smaller hem- orrhagic contusions are seen. Blood in the occipi- tal horn is present (arrow)

Discussion

Acute craniocerebral trauma may reveal several types of lesions: contusion, intracerebral and extrac- erebral hematomas, general and focal cerebral swelling, and shearing injury (diffuse axonal injury, DAI) of the cerebral white matter. The contusions are caused by direct contact between the skull and brain parenchyma, the floor of the anterior cranial fossa and most often in the temporal and frontal lobes.

Contusions also occur at sites where brain parenchy- ma impacts dural reflexion, in such locations as the splenium of the corpus callosum and dorsolateral brainstem. The contusion may be hemorrhagic or nonhemorrhagic. Hemorrhagic contusions are the most frequent lesion and may result in focal neuro- logical deficits. Contusions are much less likely to be associated with severe initial impairment of con- sciousness. When cerebral contusions are large or ex- tensive, they may act as mass lesions.

MR imaging is more sensitive in detection of brain

contusion that CT imaging. The appearance of the

contusions on MR image is variable depending upon

the constituents of the contusions. On MR imaging,

hemorrhagic contusions appeared as high signal on

T1-weighted images and as either low or high signal

on T2-weighted images, depending upon the age of

hemorrhage. The nonhemorrhagic contusion of the

brain is manifest as focal swelling and increased wa-

ter content of the brain, giving low density on CT im-

ages and prolongation on both T1- and T2-weighted

images.

Suggested Reading

Hesselink JR, Dowd CF, Healy ME, Hajek P, Baker LL, Luerssen TG (1988) MR imaging of brain contusions: a comparative study with CT. AJR Am J Roentgenol 150:1133–1142 Zimmerman RA, Bilaniuk LT, Gennarelli T, Bruce D, Dolinskas

C, Uzzell B (1978) Cranial computed tomography in diag- nosis and management of acute head trauma. AJR Am J Roentgenol 131:27–34

Diffuse Axonal Injury (DAI)

DAI in Corpus Callosum and Parenchyma Clinical Presentation

A 10-year-old female with history of car accident.

Images (Fig. 7.15)

A. T2-weighted image shows high signal involving the body and splenium of the corpus callosum (ar- row)

B. Coronal FLAIR image shows also high signal in the corpus callosum (arrow)

C. DAI appears hyperintense on b

image (SE-EPI) (arrow)

Figure 7.14 Contusion

A B

C D

D. DW image demonstrates DAI as high signal (ar- row) in the splenium. The body of the corpus cal- losum is less bright (arrowhead). A small right gray/white matter junction DAI is also present. It is best seen on DW image

E. The high signal DAI on DW image is hypointense on ADC map (arrow) representing cytotoxic ede- ma. The high signal involving the body of the cor- pus callosum represents T2-shine-through phe- nomenon. The small gray/white junction DAI is also hypointense on ADC map (arrowhead)

Figure 7.15

Diffuse axonal injury in corpus callosum and parenchyma

A B

C D E

Hemorrhagic Contusion with DAI Clinical Presentation

A 9-year-old male was involved with a car accident.

Images (Fig. 7.16)

A. Coronal T2-weighted image shows hemorrhagic contusion in the frontal lobe. Additionally the cor- pus callosum shows a vague hyperintensity repre- senting DAI

B. b

image (SE-EPI) confirms the presence of the hy- pointense hemorrhage and hyperintense edema at and above the corpus callosum

Figure 7.16

Hemorrhagic Contusion with diffuse axonal injury

A B

Multiple Areas of DAI in Corpus Callosum Clinical Presentation

A 17-year-old male with history of car accident.

Images (Fig. 7.17)

A. T2-weighted image shows hyperintense lesion in the splenium of the corpus callosum (arrow) B. Another hyperintensity is seen in the body of the

corpus callosum on T2-weighted image (arrow) C. and D.

DW images show these lesions as hyperintense (arrows)

E. and F. ADC maps show decreased signal on the DW hyperintensity (arrows) representing cytotox- ic edema

Figure 7.17

Multiple areas of diffuse axonal injury in corpus callosum

A B C

D E F

DAI with Excitotoxic Mechanism Clinical Presentation

A 12-year-old female involved in a car accident. She was referred for MR spectroscopy because of persist- ent mental status change. The conventional MR study was normal.

Images (Fig. 7.18)

A. Single voxel MR spectroscopy with TE=35ms. MR spectrum demonstrates prominent glutamate/glu- tamine peak (Glx)

B. Localizer for MR spectroscopy demonstrating the voxel placement. There is no obvious parenchymal injury

Figure 7.18

Diffuse axonal injury with excitotoxic mechanism

A B

Discussion

Diffuse axonal injury is a major form of traumatic brain injury and is caused by shearing stress prima- rily in the white matter. Diffuse axonal injury results from rotational acceleration and deceleration forces producing diffuse shear-strain deformations of brain tissue, usually at the gray/white matter junction, in the corpus callosum, and at the dorsolateral aspect of the upper brain stem. Diffuse axonal injury is usually related to general poor clinical status.

MR imaging helps in detection of pattern of injury in diffuse axonal injury. The predominant location of these injuries is the white matter of the superior frontal gyrus, at the gray/white matter interface of the frontal and temporal lobes, and in the corpus callo- sum. Most of these lesions are small (1–5mm), multi- ple, bilateral and hemorrhagic. T2-weighted gradient echo MR imaging is an excellent modality for detec- tion of small foci of hemorrhage seen in diffuse ax- onal injury. Diffusion-weighted imaging shows areas of increased signal with decreased ADC value.

Blunt trauma is a mechanism that elevates the ex- tracellular glutamate levels. This triggers the excito- toxic cascade by allowing excessive accumulation of glutamate in the synaptic space. This can produce disastrous results in the neurons leading to neuronal death. One recent therapeutic approach is to use glu- tamate receptor blockers to minimize neuronal death.

Suggested Reading

Liu AY, Maldjian JA, Bagley LJ, Sinson GP, Grossman RI (1999) Traumatic brain injury: diffusion-weighted MR imaging findings. AJNR Am J Neuroradiol 20:1636–1641

Mark LP, Prost RW, Ulmer JL, et al (2001) Pictorial review of glutamate excitotoxicity: fundamental concepts for neu- roimaging. AJNR Am J Neuroradiol 22:1813–1824 Scheid R, Preul C, Gruber O,Wiggins C, von Cramon DY (2003)

Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2-weighted gradient-echo imaging at 3T. AJNR Am J Neuroradiol 24:1049–1056 Tong KA, Ashwal S, Holshouser BA, et al (2003) Hemorrhagic

shearing lesions in children and adolescents with post-

traumatic diffuse axonal injury: improved detection and

initial results. Radiology 227:332–339

Periventricular Leukomalacia (PVL),

Preterm Hypoxic Ischemic Encephalopathy (HIE)

Periventricular Leukomalacia with White Matter Aplasia Clinical Presentation

A 3-year-old female, former 33-week gestational age premature baby has developmental delay and spastic diplegia. She presents because of frequent falls.

Images (Fig. 7.19)

A. T2-weighted image shows gray matter extending to the ventricles (arrows) from severe white matter loss, mainly in the posterior aspect of the brain.

Undulation of the ventricular walls is seen. De- myelination of the external capsule is seen (arrow- head)

B. FLAIR image shows periventricular and external capsule demyelination. Again undulation of the ventricular walls is present. Thin genu of corpus callosum is seen

C. Sagittal T1-weighted image shows hypoplasia of the corpus callosum (arrow) and cingulate gyrus

Figure 7.19

Periventricular leukomalacia with white matter aplasia

A B

C

Periventricular Leukomalacia with Thin Corpus Callosum Clinical Presentation

A 12-month-old girl with developmental delay, mixed tone and past history of 33weeks prematurity with respiratory distress syndrome.

Images (Fig. 7.20)

A. Sagittal T1-weighted image shows thin corpus cal- losum

B. Proton density image reveals characteristic en- largement of the ventricles with irregular borders and periatrial hyperintensity representing white matter gliosis (arrows)

C. T1-weighted image shows deep sulci abutting the irregular ventricles

D. T2-weighted image shows characteristic periatrial gliosis (arrows) with deep sulci and white matter volume loss

Figure 7.20

Periventricular leukomalacia with thin corpus callosum

A B

C D

Unilateral Periventricular Leukomalacia Clinical Presentation

A 2-year-old ex-premature male with left hemipare- sis and developmental delay.

Images (Fig. 7.21)

A. Gray matter indents the ventricle wall (arrow) due to severe white matter loss on right. Corpus callo- sum is thin. The right hemisphere is smaller than the left. Typical undulation of ventricular wall is present

Periventricular Leukomalacia

with Dystrophic Parenchymal Calcification Clinical Presentation

A 7-month-old female with developmental delay and a remote history of cardiac arrest and renal failure.

Images (Fig. 7.22)

A. Sagittal T1-weighted image shows thin corpus cal- losum

B. Proton density image reveals white matter volume loss with low signal calcification (arrows) in the frontal region

C. The parenchymal calcification is well seen on SPGR image (arrows)

Discussion

Periventricular leukomalacia (PVL) (synonym:

preterm hypoxic-ischemic encephalopathy, HIE) in a preterm infant (32–36weeks) results from extensive necrosis of white matter adjacent to the lateral ven- tricles in the brain. Before 32weeks gestational age (28–32weeks), germinal matrix, intraventricular and intraparenchymal hemorrhages are more common.

PVL is seen in 70% of preterm infants with HIE. The determining factor for different patterns of ischemia at the CNS is the time of the anoxic insult. Before 32weeks gestational age, cavitary PVL and hemor- rhages prevail. PVL is rarely seen in term neonates. In term infants the pattern of damage is different. The HIE in term infants is seen in parasagittal, cortical and subcortical regions. In preterm infants the deep periventricular white matter is thought to be at the highest risk of ischemic insult before maturation of centrifugal arteries. Significant risk factors in addi- tion to prematurity include premature rupture of membranes, chorioamnionitis and hyperbilirubine- mia. Clinical manifestations include spastic diplegia, quadriparesis, visual disorders, seizures, and cogni- tive disorders.

Although, ultrasound (US) imaging is used in the acute phase which detects hyperechoic periventricu- lar areas, MR imaging is superior in detection of white matter loss and delayed myelination. The most common findings observed are: abnormally in- creased periventricular white matter intensity on T2- weighted image, commonly seen in the trigone re-

Figure 7.21

Unilateral periventricular leukomalacia

gions of lateral ventricles, marked loss of periventric- ular white matter predominantly in periatrial re- gions, and compensatory focal ventricular enlarge- ment adjacent to regions of abnormal signal intensi- ty. Typically the late findings consist of undulation of ventricular surface, periventricular cysts, callosal thinning, evidence of prior hemorrhage and gliosis.

DW images may show signal hyperintensity associat- ed with decreased ADC values. DW imaging may have a higher correlation with later evidence of PVL than conventional MR imaging when performed in the acute phase. Imaging recommendations in sus- pected cases include early US screening and then MR imaging with DW imaging and MR spectroscopy.

Suggested Reading

Barkovich AJ, Westmark K, Partidge C, Sola A, Ferriero DM (1995) Perinatal asphyxia: MR findings in the first 10 days.

AJNR Am J Neuroradiol 16:427–438

Bozzao A, Di Paolo AD, Mazzoleni, et al (2003) Diffusion- weighted MR imaging in the early diagnosis of periven- tricular leukomalacia. Eur Radiol 13:1571–1576

Wilson DA, Steiner RE (1986) Periventricular leukomalacia:

evaluation with MR imaging. Radiology 160:507–511 Figure 7.22

Periventricular leukomalacia with dystrophic parenchymal calcifica- tion

A B

C

Figure 7.23

Hypoxic ischemic encephalopathy with infarcts

A B

C D

Hypoxic Ischemic Encephalopathy (HIE)

Hypoxic Ischemic Encephalopathy with Infarcts Clinical Presentation

A 6-day-old full term neonate with traumatic birth and low Apgar scores. Patient is spastic.

Images (Fig. 7.23)

A. T2-weighted image reveals hyperintense and in- distinct cortical gray matter ribbon in both MCA territories (arrows)

B. Contrast-enhanced T1-weighted image reveals vague enhancement in both MCA territories C. DW image shows significant hyperintensity main-

ly in both MCA territories and in the splenium of the corpus callosum

D. The hyperintense lesions on DW image are hy- pointense on ADC map consistent with restricted diffusion and cytotoxic edema often seen in is- chemic damage

Hypoxic Ischemic Encephalopathy with Brain Edema

Clinical Presentation

A 9-day-old female infant with hypoglycemia and seizures.

Images (Fig. 7.24)

A. Noncontrast CT scan shows diffuse brain edema, more in the occipital area

B. T1-weighted image shows cortical hyperintensi- ties representing laminar necrosis

C. T2-weighted image shows intense bilateral poste- rior parietal hyperintensity with loss of cortical ribbon (arrows)

D. FLAIR image confirms the laminar necrosis (ar- rows)

Hypoxic Ischemic Encephalopathy Post-Surgery Clinical Presentation

A previously healthy 4-year-old female who experi- enced two seizures leading to anoxia after a minor elective surgery.

Images (Fig. 7.25)

A. Contrast enhanced T1-weighted image shows mild hypointensities in the bilateral frontal and occipi- tal lobes (arrows) in watershed distribution B. DW image shows hyperintense lesions in the bilat-

eral frontal and occipital lobes (arrows)

Figure 7.24

Hypoxic ischemic encephalopa- thy with brain edema

A B

C D

Figure 7.25

Hypoxic ischemic encephalopa- thy post-surgery

A B

Hypoxic Ischemic Encephalopathy with Seizures

Clinical Presentation

A 15-year-old male with seizure followed by cardiac arrest and decreased mental status.

Images (Fig. 7.26)

A. T2-weighted image reveals significant hyperinten- sity in both the putamina and the head of the cau- date nuclei. The cortical ribbon and gray/white matter junction are indistinct in both occipital lobes

B. Coronal FLAIR confirms the putaminal and cau- date hyperintensities. It also reveals focal subcorti- cal white matter hyperintensities

C. Contrast-enhanced T1-weighted image (with magnetization transfer) shows patchy occipital enhancement

D. DW image shows significant hyperintensity in- volving the putamina, medial thalami, both occip- ital cortices and superior temporal gyri. Wedge- shaped hyperintensity is seen in insular cortices with relative sparing of the frontal lobes

Figure 7.26

Hypoxic ischemic encephalopa- thy with seizures

A B

C D

Discussion

HIE in term infants is an acquired condition in which signs of fetal distress are present prior to delivery, the infant has low Apgar scores, requires resuscitation at birth and has neurological symptoms during the first 24hours of life. The early recognition, prompt med- ical intervention, and accurate prognostic prediction of perinatal brain damage are particularly important to decrease morbidity and mortality in affected in- fants. MR imaging has a large impact on the evalua- tion of the asphyxiated neonate.

In mild hypoperfusion injury there is redistribu- tion of cerebral blood flow to vital structures in the basal ganglia, brainstem and cerebellum. The white matter is damaged with sparing of the vital gray mat- ter structures. In more profound hypoperfusion, the cerebral blood flow has no time to shift and areas of highest metabolic needs such as the basal ganglia will be damaged. The deep gray matter has been thought to be vulnerable to selective neuronal necrosis in acute total asphyxia. Often the damage is mixed.

Injury in the perinatal period in term infants shows short T1 and T2 in the ventral lateral thalami, posterolateral lentiform nuclei, posterior mesen- cephalon, and hippocampi, and asphyxia later in in- fancy shows prolonged T2 in the corpus striatum and most of the cerebral cortex with perirolandic spar- ing. In term infants diffuse hemispheric parenchymal changes have been associated with severe prolonged partial asphyxia when there is repetitive stress with intermittent recovery. Focal hemispheric changes in the form of infarction may be seen.

Neonatal hypoglycemia is caused by imbalance be- tween supply and utilization of glucose. It can lead to HIE and metabolic strokes. Risk factors include pre- maturity, mother’s diabetes, maternal use of steroids, toxemia, infant sepsis and hypoxia. The classic imag- ing appearance is that of T2 or FLAIR hyperintensity on the occipito-parietal area posteriorly or DW im- aging hyperintensity with hypointense ADC map in the same area. MR spectroscopy is helpful in early is- chemia. Glutamine/glutamate peaks are increased in ischemia. Lactate is a normal finding in a developing brain (<37weeks) as is a low NAA peak.

HIE is not limited to the perinatal period. In older children HIE can follow cardiac arrest, seizures, suf- focation, drowning and other condition where hy- poxia is present. In all cases of HIE standard MR im- ages may be normal up to 72hours. However, DW im- aging with ADC map is very sensitive in early imag- ing of ischemia, but the findings pseudonormalize

within a week. MR spectroscopy is helpful in early stages of ischemia demonstrating increased gluta- mine/glutamate peaks.

In preterm infants the ischemic damage is differ- ent. Before 32weeks of gestational age MR imaging can show parenchymal and intraventricular hemor- rhage. At 32–36weeks of gestational age periventric- ular white matter damage (PVL) and deep gray matter involvement is commonly seen. Subependy- mal hemorrhage is one of the common sequelae in premature infants which may be depicted as periventricular hemosiderin deposits on initial MR images. Parenchymal encephaloclastic cysts adjacent to hemosiderin deposits may be seen in follow-up MR images. Diffusion tensor imaging may show significant reduction of fractional anisotropy in the posterior limb of the internal capsule.

Suggested Reading

Aida N, Nishimura G, Hachiya Y, Matsui K, Takeuchi M, Itani Y (1998) MR imaging of perinatal brain damage: compari- son of clinical outcome with initial and follow-up MR find- ings. AJNR Am J Neuroradiol 19:1909–1921

Arzoumanian Y, Mirmiran M, Barnes PD, et al (2003) Diffusion tensor brain imaging findings at term-equivalent age may predict neurologic abnormalities in low birth weight preterm infants. ANJR Am J Neuroradiol 24:1646–1653 Barkovich AJ (1992) MR and CT evaluation of profound

neonatal and infantile asphyxia. AJNR Am J Neuroradiol 13:959–972

Barkovich AJ, Westmark K, Partridge C, Sola A, Ferriero DM (1995) Perinatal asphyxia: MR findings in the first 10 days.

AJNR Am J Neuroradiol 16:427–438

Hypoxic Encephalopathy in Near-Drowning Clinical Presentation

A 3-year-old boy, near-drowning victim found in swimming pool. The study was obtained 4days after the accident.

Images (Fig. 7.27)

A. T2-weighted image shows partially hemorrhagic, partially necrotic lesions in the globus pallidi (ar- rows), caudate nuclei and posterior putamen B. FLAIR image confirms the necrotic findings in

globus pallidi

C. T2-weighted image through the midbrain reveals hyperintensity involving the corticospinal tracts, compact substantia nigra and periaqueductal gray matter (arrowhead). Mamillary bodies also demonstrate abnormal hyperintensity (arrows) D. FLAIR image shows hyperintensity in the caudate

body

Figure 7.27

Hypoxic encephalopathy in near- drowning

A B

C D

Discussion

Drowning is defined as death by asphyxia due to sub- mersion in a liquid medium. The term “near-drown- ing” is applied to patients with cardiac arrest and as- phyxia after submersion in water, who are resuscitat- ed and survive beyond 24hours. Of those who survive prolonged submersion, the majority have severe neu- rological impairment, but as many as 30% may re- main neurologically intact. During a drowning episode, neurological damage may be caused by a va- riety of factors, including cerebral hypoxia, carbon dioxide narcosis, laryngospasm, pulmonary reflexes, or vagally mediated cardiac arrest.

MR imaging findings include focal (particularly occipital) and generalized edema, basal ganglia changes, cortical abnormalities, and brain stem in- farcts. The earliest basal ganglia changes are of dif- fuse T1 hyperintensities, which may be seen as early as 1day after the hypoxic event. Later, the areas of hy- perintensity become more focal and show a charac- teristic distribution involving the posterior lentiform nuclei and ventrolateral thalamus. The indistinct basal ganglia margins on T2-weighted images are a common finding and are an early sensitive indicator of an anoxic-ischemic event. In the first 24hours, the presence of edema or T2 changes in the basal ganglia is both sensitive and specific for poor outcome. In se- vere cases, the basal ganglia margins may progress to invisible basal ganglia. In infants, laminar necrosis occurs more commonly and high intensity subcorti- cal lines are more frequent in older children.

DW imaging with ADC map often depicts acute or subacute ischemic brain lesions when CT and MR images are normal or near normal. The prognosis of HIE depends on the severity and extension of the le- sions. Since cytotoxic edema is usually irreversible, DW is helpful in estimating a patient’s prognosis and management, especially if it is combined with MR spectroscopy. MR imaging and MR spectroscopy are complementary studies and they measure different aspects of hypoxia. Gray matter MR spectroscopy in cases with poor outcome shows a markedly de- creased NAA peak and elevation of glutamine/gluta- mate and lactate.

Suggested Reading

Dubowitz DJ, Bluml S, Arcinue E, Dietrich RB (1998) MR of hy- poxic encephalopathy in children after near-drowning:

correlation with quantitative proton MR spectroscopy and clinical outcome. AJNR Am J Neuroradiol 19:1617–1627 Kreis R,Arcinue E, Ernst T, Shonk TK, Flores R, Ross BD (1996)

Hypoxic encephalopathy after near-drowning studied by quantitative 1H-magnetic resonance spectroscopy. J Clin Invest 97:1142–1154

Multicystic Encephalomalacia Clinical Presentation

A 3-month old male with history of right hemispher- ic stroke.At the age of 3years he presents in the emer- gency room with seizures.

Images (Fig. 7.28)

A. T1-weighted image shows a thin corpus callosum B. DW image shows hypointensity in right hemi-

sphere cystic lesions

C. Axial FLAIR image reveals small right hemisphere and multiple CSF containing spaces with dilated lateral ventricle

D. Coronal FLAIR image confirms the encephaloma- lacia and ex vacuo atrophy displacing the midline to right

E. T2-weighted image shows diffuse hyperintense cysts throughout the right hemisphere that is smaller

F. T1-weighted image shows hypointensity in the right cerebral hemisphere. This is consistent with an area of encephalomalacia and gliosis due to a prior insult such as infarct or infection. Minimal hyperintensity is noted in the area of encephalo- malacia consistent with mineralization

G. T1-FLAIR image shows multiple CSF containing cysts. The thin cortex is better appreciated in this sequence

H. CT at the age of 3years shows multicystic en- cephalomalacia with small right hemicranium

Figure 7.28

Multicystic encephalomalacia

A B

C D E

F G H

Discussion

The developing brain is susceptible to injury from in- fectious, ischemic and inflammatory insults. Multi- cystic encephalomalacia results from insult to the brain late in gestation, during birth or after birth. En- cephalomalacia, in contradistinction to poren- cephaly, is characterized by astrocytic proliferation and glial septations within the damaged brain. The location of the cysts varies with the nature of the le- sion. In the early 1980s, diagnosing periventricular (PVL) and multicystic leukomalacia in neonates us- ing cranial sonography was possible for the first time.

The more wide use of MR imaging in the late 1980s allowed more detailed brain imaging even in small preterm babies often vulnerable to brain injury from many causes. MR imaging being more accurate shows more numerous or more extensive cysts compared to US studies. MR images are also able to show cysts not present on sonograms. CT scans show initially hy- pointensity leading later to cyst formation. Calcifica- tion may be present. On early MR images ill-defined T1 and T2 prolongation is present leading later to multiple cystic lesions with strands of glial septae.

MR spectroscopy shows low metabolites.

Suggested Reading

Inder TE, Anderson NJ, Spencer C, Wells S, Volpe JJ (2003) White matter injury in the premature infant: a comparison between serial cranial sonographic and MR findings at term. AJNR Am J Neuroradiol 5:805–809

Resch B, Vollaard E, Maurer U, Haas J, Rosegger H, Muller W (2000) Risk factors and determinants of neurodevelop- mental outcome in cystic periventricular leucomalacia.

Eur J Pediatr 9:663–670

Status Epilepticus and Postictal Stage Status Epilepticus

with Partially Reversible Tissue Changes Clinical Presentation

A 19-year-old male who has epilepsy, had an episode of status epilepticus. Patient was transferred from an outside hospital due to prolonged status epilepticus.

He is still having impaired cognitive function after 5days of ictus and hypoxic injury is suspected clini- cally.

Images (Fig. 7.29)

A. There is diffuse increased signal intensity in the right temporal parietal cortex and right hip- pocampus (arrows). The cortex is swollen

B. On coronal FLAIR image the hippocampus is hy- perintense and swollen (arrow). Cortical swelling is also demonstrated

C. On DW image the same areas are hyperintense D. ADC values are decreased in these areas, confirm-

ing restricted diffusion E. and F.

In the follow-up study 12days later the large diffu- sion abnormality involving the right temporal and parietal cortices has largely resolved

G. and H.

There is persistent gyral swelling and T2 prolon-

gation involving the right temporal cortex seen on

axial T2-weighted (G) and coronal FLAIR (H) im-

ages

Figure 7.29 A–H

Status epilepticus with partially reversible tissue changes

A B

C D E

G

F H

Status Epilepticus

with Permanent Tissue Damage Clinical Presentation

A 2-year-old female with Rasmussen’s encephalitis and developmental delay presents with focal seizures involving the right face and hand. The girl subse- quently underwent hemispherectomy.

Images (Fig. 7.30)

A. On T2-weighted image there is diffuse thalamic and cortical hyperintensity on the left side B. Coronal FLAIR image shows better the abnormal

increased signal within the swollen gyri

C. DW image shows a gyriform area of high signal involving the thalamus and entire cortical area on the left side

D. ADC values are decreased in hyperintense lesion on DW image (C), confirming restricted diffusion as seen in cytotoxic edema

E. Contrast-enhanced image demonstrates slight hy- peremia on the left

F. MR angiography (noncontrast study, 3D TOF) shows increased flow-related enhancement on the left MCA, especially at the peripheral branches (arrowheads). The left MCA is also dilated (arrow) consistent with hyperperfusion

G. Single voxel proton MR spectroscopy on the left side 9days later shows questionable lactate peak.

There is increased choline with relatively low NAA compared to the uninvolved right side. Short echo MR spectroscopy showed increased glutamine/

glutamate peaks (not shown)

H. Localizer for the MR spectroscopy demonstrating the analyzed voxel

I. DW image 9days later shows a gyriform area of high signal involving mainly the occipital cortex on the left side. The frontoparietal cortex is near normal

J. The corresponding ADC map shows still hy- pointensity in the occipital area (arrow). The fron- toparietal hypointensity on the initial study (D) is near normal

K. T2-weighted image 5months later shows interval increase in the ventricular size especially on the left temporal and parietal lobes with no associated sulcal effacement. This is consistent with tissue loss. There is a persistent hyperintensity of the left hemisphere on T2-weighted images

L. On contrast-enhanced image, there is persistent enhancement of the gray matter of the left cerebral hemisphere especially in the occipital region M.DW image shows no abnormal signal N. ADC map shows parenchymal hyperintensity

Discussion

MR imaging is widely used to evaluate patients with seizures. In the early development of MR imaging the studies were obtained to detect anatomical, develop- mental and structural brain abnormalities and eval- uate patients for seizure surgery. MR imaging is espe- cially useful in the diagnosis of mesial temporal scle- rosis. Also parahippocampal structures are well visu- alized in MR imaging. On the standard MR image, signal alterations related to ictal or postictal situation can be misdiagnosed as cerebritis, infarctions, MELAS, herpes encephalitis, neoplastic lesions or even demyelinating diseases. DW imaging is helpful in evaluating patients with epilepsy, as it will dis- criminate between cytotoxic edema and vasogenic edema in ictal and postictal brain. Standard MR im- aging can demonstrate transient increase in T2 signal and cortical swelling in addition to hippocampus, corpus callosum, thalamic and cerebellar signal alter- ations. During ictus there is increased metabolic ac- tivity and consumption of oxygen and glucose in the seizure focus. This hypermetabolic state results in metabolic ischemia, hypercarbia and lactic acidosis, which impair vascular autoregulation in the affected areas leading to vasogenic edema and disruption of the blood-brain barrier.

If the patient suffers from a continuous seizure

lasting longer than 30minutes or two or more con-

secutive seizures together lasing longer than 30min-

utes without full recovery, the situation is called sta-

tus epilepticus. This is a serious condition. Several in-

vestigators have found reversible lesions in MR im-

ages after status epilepticus. Research has shown that

there is increase in the release of glutamate from the

presynaptic terminal of neuronal axons. Cytotoxic

edema in status epilepticus and acute ischemia pres-

ents with restricted diffusion. A cascade of events in

status epilepticus result in cytotoxic edema that can

Figure 7.30 A–G

Status epilepticus with permanent tissue damage (H–N see next page)

A B

C D E

F G

Figure 7.30 H–N

Status epilepticus with permanent tissue damage

H I J

K L M

N

be at least partially reversible. This is in contrast to considerable ischemia where changes are usually ir- reversible. In the ischemic process there is significant compromise of the blood supply to the brain; howev- er, in status epilepticus there is an increase in cerebral metabolism with an increase in the blood flow seen in MR angiography and MR perfusion studies. This will maintain the energy supply of the neurons provided that there is sufficient oxygen supply. Although some lesions are reversible, most lesions in status epilepti- cus are permanent with neuronal necrosis, gliosis and delayed neuronal death with subsequent atrophy.

DW imaging and ADC maps are more sensitive than conventional MR imaging to visualize gray and white matter involvement and discriminate between cytotoxic and vasogenic edema following status epilepticus. DW image reveals an acute postictal de- pression of ADC (low signal), interictal normaliza- tion and then chronic elevation (high signal) in the seizure focus. Distinction between vasogenic and cy- totoxic edema is important since cytotoxic edema following a seizure indicates more extensive brain damage that is often irreversible leading to tissue loss and atrophy.

Suggested Reading

Bronen RA (2000) The status of status: seizures are bad for your brain’s health. AJNR Am J Neuroradiol 21:1782–1783 Flacke S, Wullner U, Keller E, Hamzei F, Urbach H (2000) Re- versible changes in echo planar perfusion- and diffusion- weighted MRI in status epilepticus. Neuroradiology 42:92–95

Kim JA, Chung JI, Yoon PH, et al (2001) Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imag- ing. AJNR Am J Neuroradiol 22:1149–1160

Cortical Laminar Necrosis Clinical Presentation

A 6-month-old male who suffered status epilepticus, brain edema followed with subsequent diffuse vol- ume loss and laminar necrosis.

Images (Fig. 7.31)

A. Sagittal T1-weighted image reveals characteristic laminar hyperintense lesions of the cerebral cor- tex (arrows)

B. Significant volume loss is seen on T2-weighted im- age, especially in the fontal lobes

C. Coronal T2-weighted image shows significant cor- tical atrophy, thinning of the corpus callosum and extensive white matter changes that are often pro- gressive

Discussion

Cortical laminar necrosis is a histopathological enti- ty, related to conditions of cerebral energy depletion, especially hypoxia-ischemia and hypoglycemia, ei- ther in the perinatal period or later in life. Neurons are more vulnerable to energy depletion than glial cells and vascular elements, and among the layers of gray matter, the third layer is more vulnerable than superficial layers. White matter abnormalities tend to be more frequent in premature children, and cortical laminar abnormalities tend to be more common in term neonates and older children.

Cerebral edema is seen in the acute stage. Early

cortical changes usually show low signal intensity on

T1-weighted MR images which could be due to acute

ischemic changes. Unenhanced T1-weighted images

reveal characteristic laminar hyperintense lesions of

the cerebral cortex in the late subacute stage. Usually,

cortical high-intensity lesions on both T1-weighted

and FLAIR images appear 2weeks after the ictus, in-

dicating short T1 and long T2 lesions. On proton den-

sity images, cortical laminar necrosis may be seen as

high intensity due to increased mobile protons in the

reactive tissue. In the chronic stage, cortical atrophy

and delayed but progressive white matter changes are

present.

In severe HIE, subtle changes may be difficult to see with conventional MR imaging. DW images are helpful for evaluating and dating diffuse cerebral anoxia, and therefore aid in the determination of prognosis and management of these patients. During the acute period, DW images may show abnormali- ties in the basal ganglia, cerebellum, and cortex. Dur- ing the early subacute period, gray matter abnormal- ities dominate in the DW images. During the late sub- acute period, DW images may show mostly white matter abnormalities. During the chronic stage, the results of DW imaging are normal, but conventional MR imaging shows laminar necrosis, atrophy and volume loss.

Suggested Reading

Komiyama M, Nishikawa M, Yasui T (1997) Cortical laminar necrosis in brain infarcts: chronological changes on MRI.

Neuroradiology 39:474–479

Valanne L, Paetau A, Suomalainen A, Ketonen L, Pihko H (1996) Laminar necrosis in MELAS syndrome: MR and neu- ropathological observations. Neuropediatrics 27:154–160 Van der Knaap MS, Smit LS, Nauta JJ, Lafeber HN,Valk J (1993)

Cortical laminar abnormalities – occurrence and clinical significance. Neuropediatrics 24:143–148

Figure 7.31

Cortical laminar necrosis

A B

C

Cyclosporin-Induced Encephalopathy Clinical Presentation

A 1-year-old male with altered mental status and muscle weakness following cyclosporin treatment.

Images (Fig. 7.32)

A. T2-weighted image shows extensive white matter hyperintensity with some gray matter involve- ment and insular cortex involvement. No mass ef- fect is present

B. T2-weighted image through the centrum semio- vale shows near complete involvement of the white matter with some cortical gray matter involve- ment on the left

C and D. T1-weighted image with contrast enhance- ment shows diffuse white matter enhancement

Discussion

The incidence of cyclosporin-induced neurotoxicity has been reported to be 10–25%. Endothelial injury is thought to be the main causative factor. The clini- cal features may include headache, tremor, hallucina- tions, and altered level of consciousness, seizures, cerebellar ataxia, transient aphasia, muscle weakness and visual disturbance. Cyclosporin-induced toxicity is often reversible.

Both cortical gray and white matter involvement has been described. CT images show hypodense areas in the subcortical white matter or gray matter. Focal subcortical areas of hemorrhage may be seen in ad- vanced cases. T2-weighted images typically show ar- eas of high signal intensity in the subcortical white matter mainly in the occipital-parietal regions.

Rarely, other locations such as the frontal lobes, cor- pus callosum, brain stem, pons and cerebellum may also be involved. The cortical gray matter can also be involved. Cortical laminar necrosis has been de-

Figure 7.32 Cyclosporin-induced encephalopathy

A B

C D